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排序方式: 共有632条查询结果,搜索用时 15 毫秒
1.
Maria Gonzalez-Cao Cristina Carrera Juan Francisco Rodriguez Moreno Pedro Rodríguez-Jiménez Mónica Antoñanzas Basa Rosa Feltes Ochoa Teresa Puertolas Eva Muñoz-Couselo José Luis Manzano Ivan Marquez-Rodas Juan Martín-Liberal Ainara Soria Pilar Lopez Criado Almudena Garcia-Castaño Aram Boada Pablo Ayala de Miguel Susana Puig Guillermo Crespo Alfonso Berrocal 《Journal of the American Academy of Dermatology》2021,84(5):1412-1415
2.
S Amartur Z P Liang F Boada E M Haacke 《Journal of magnetic resonance imaging : JMRI》1991,1(6):721-724
The authors present an improvement to a sigma-filter extrapolation method for the reconstruction of magnetic resonance (MR) images from symmetric discrete Fourier data. By making use of the phase information in the image data, the proposed method can overcome the data inconsistency problem of the original method for handling MR image data with large phase variations, such as those obtained in gradient-echo pulse sequences. Reconstruction results show that its performance is comparable with that of the modified complex sigma-filter method proposed previously to handle the inconsistency problem. However, the new approach has the advantage of reducing computation time by a factor of two with use of a sigma filter applied to real instead of complex images. It is expected that this method will be more practical for use in clinical MR imaging systems. 相似文献
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Mutations in APP are associated with familial early-onset Alzheimer disease (FAD). Examination of the genomic sequence in one patient with FAD revealed a change located in the axon 17 of the APP gene at position 275329G>A (GenBank accession number: D87675; GI: 2429080); cDNA sequence 2137G>A (GenBank accession number: X06989; GI: 28720). This corresponds to the mutation A713T in APP. AD stage VI of neurofibrillary degeneration and stage C of Aβ-amyloid burden was found at the post-mortem neuropathological examination. Previous studies have suggested that the mutation A713T in APP is a silent mutation or polymorphism. However, we have not found this change in APP in a control population analyzed by the amplification-refractory mutation system (ARMS). It is concluded that A713T in APP is implicated in the pathogenesis of AD. Since the immunohistochemical study indicates that A713T mutation is not likely to relate with Aβ-amyloid processing, the causative role of this rare mutation remains to be warranted. 相似文献
8.
Jennifer Janusz Caroline Harrison Cristina Boada Lisa Cordeiro Susan Howell Nicole Tartaglia Richard Boada 《American journal of medical genetics. Part C, Seminars in medical genetics》2020,184(2):469-481
Few studies have systematically assessed executive functioning (EF) skills in boys with XXY, and these are limited by small samples and restricted EF assessment. This study used a broader battery of performance‐based measures as well as parent‐rating scales of EF in 77 boys and adolescents with XXY (mean age = 12.5 years), recruited from a clinical trial and an outpatient clinic. Exploratory factor analyses were used to create EF domains from performance‐based measures, and similar domains were measured using the Behavior Rating Inventory of Executive Function and Conners Parent‐Rating Scales. The boys with XXY showed a distinct EF profile, with the greatest deficit in attention and more moderate deficits in working memory, switching, and planning/problem solving. Parent ratings showed similar challenges, as well as impaired inhibition. Independent sample t‐tests showed no difference on performance measures between boys diagnosed or not diagnosed with attention‐deficit/hyperactivity disorder (ADHD), although parents of boys diagnosed with ADHD reported more difficulties. There were no differences on performance‐based tests between those diagnosed pre‐ and postnatally, although parents of postnatally diagnosed boys reported more metacognitive problems. Language deficits, cognition, and socio‐economic status did not account for EF deficits. 相似文献
9.
Jolinda LD Schram Joost Oude Groeniger Merel Schuring Karin I Proper Sandra H van Oostrom Suzan JW Robroek Alex Burdorf 《Scandinavian journal of work, environment & health》2021,47(2):127
Objective:Using a novel mediation method that presents unbiased results even in the presence of exposure–mediator interactions, this study estimated the extent to which working conditions and health behaviors contribute to educational inequalities in self-rated health in the workforce.Methods:Respondents of the longitudinal Survey of Health, Ageing, and Retirement in Europe (SHARE) in 16 countries were selected, aged 50–64 years, in paid employment at baseline and with information on education and self-rated health (N=15 028). Education, health behaviors [including body mass index (BMI)] and working conditions were measured at baseline and self-rated health at baseline and two-year follow-up. Causal mediation analysis with inverse odds weighting was used to estimate the total effect of education on self-rated health, decomposed into a natural direct effect (NDE) and natural indirect effect (NIE).Results:Lower educated workers were more likely to perceive their health as poor than higher educated workers [relative risk (RR) 1.48, 95% confidence interval (CI) 1.37–1.60]. They were also more likely to have unfavorable working conditions and unhealthy behaviors, except for alcohol consumption. When all working conditions were included, the remaining NDE was RR 1.30 (95% CI 1.15–1.44). When BMI and health behaviors were included, the remaining NDE was RR 1.40 (95% CI 1.27–1.54). Working conditions explained 38% and health behaviors and BMI explained 16% of educational inequalities in health. Including all mediators explained 64% of educational inequalities in self-rated health.Conclusions:Working conditions and health behaviors explain over half of the educational inequalities in self-rated health. To reduce health inequalities, improving working conditions seems to be more important than introducing health promotion programs in the workforce. 相似文献
10.
Characterization of xenobiotic-metabolizing enzymes and nitrosamine metabolism in the human esophagus 总被引:5,自引:2,他引:5
Smith TJ; Liao A; Wang LD; Yang GY; Starcic S; Philbert MA; Yang CS 《Carcinogenesis》1998,19(4):667-672
Esophageal cancer has been associated with tobacco smoking, and
nitrosamines are possible causative agents for this cancer. The present
study investigated the metabolism of the tobacco carcinogens N'-
nitrosonornicotine (NNN), 4-(methylnitrosamino)-1-(3-pyridyl)-1- butanone
(NNK), and N-nitrosodimethylamine (NDMA), as well as the presence of
xenobiotic-metabolizing enzymes in human esophageal tissues from
individuals in the United States and Huixian, Henan Province, China (a
high-risk area for esophageal cancer). All esophageal microsomal samples
activated NNN and the metabolic rate was 2-fold higher in the esophageal
samples from China than the USA. All microsomal samples activated NDMA.
However, most of the microsomal samples did not activate NNK.
Troleandomycin (an inhibitor of cytochrome P450 3A) decreased the formation
of NNN-derived keto acid by 20-26% in the esophageal microsomes. The
activities for NADPH: cytochrome c reductase, ethoxycoumarin O-deethylase,
NAD(P)H: quinone oxidoreductase and glutathione S-transferase were present
in the esophageal samples. Coumarin 7-hydroxylase (a representative
activity for P450 2A6) activity was not detected in the esophageal
microsomal samples. The activities for nitrosamine metabolism and
xenobiotic- metabolizing enzymes were decreased (by 30-50%) in the squamous
cell carcinomas compared with their corresponding non-cancerous mucosa. The
presence of activation and detoxification enzymes in the esophagus may play
an important role in determining the susceptibility of the esophagus to the
carcinogenic effect of nitrosamines. Our results suggest that P450s 3A4 and
2E1 are involved in the activation of NNN and NDMA, respectively, in the
human esophagus.
相似文献